Chronic Pharmacological Increase of Neuronal Activity Improves Sensory-Motor Dysfunction in Spinal Muscular Atrophy Mice

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¹Carl-Ludwig-Institute for Physiology, Leipzig University, Leipzig 04103, Germany
²Rudolf-Schönheimer Institute for Biochemistry, Leipzig University, Leipzig 04103, Germany
³Center for Motor Neuron Biology and Disease, Columbia University, New York, New York 10032
⁴Departments of Pathology and Cell Biology and Neurology, Columbia University, New York, New York 10032

E. V. Fletcher's present address: Oncogenic Signaling Laboratory, Telethon Kids Institute, Perth Children's Hospital, Nedlands, Western Australia 6009, Australia.

Author contributions: C.M.S. and G.Z.M. designed research; C.M.S., B.B.-R., J.M.B., J.G.P., E.V.F., and J.K.S.L. performed research; C.M.S., B.B.-R., J.M.B., J.G.P., E.V.F., and J.K.S.L. analyzed data; C.M.S. and G.Z.M. wrote the paper.

E. V. Fletcher's present address: Oncogenic Signaling Laboratory, Telethon Kids Institute, Perth Children's Hospital, Nedlands, Western Australia 6009, Australia.

This work was supported by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) Grant SI-1969/2-1 (to C.M.S.). G.Z.M. was supported by the National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health (NIH) Grant R01-NS078375, The NIH Blueprint for Neuroscience Research, the National Institute on Alcohol Abuse and Alcoholism and NINDS Grant R01-AA027079, The SMA Foundation, and Project-ALS. We thank Dr. Livio Pellizzoni for helpful comments. We also thank Dr. Stefan Hallermann, Dr. Johannes Hirrlinger, and Dr. Tobias Langenhan for providing reagents and facility access.
The authors declare no competing financial interests.
Correspondence should be addressed to Christian M. Simon at christian.simon{at}medizin.uni-leipzig.de

HHS | NIH | National Institute of Neurological Disorders and Stroke (NINDS)
R01-NS078375; R01-AA027079
Project ALS
SAM Foundation
Deutsche Forschungsgemeinschaft (DFG)
SI-19692